In vivo axonal transport rates decrease in a mouse model of Alzheimer's disease
In vivo axonal transport rates decrease in a mouse model of Alzheimer's disease
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DOI：
10.1016/j.neuroimage.2007.01.046
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发表时间：
2007-05-01
期刊：
影响因子：
5.7
通讯作者：
Pautler, Robia G.
中科院分区：
文献类型：
--
作者：
Smith, Karen Dell Brown;Kallhoff, Verena;Pautler, Robia G.
轴突病是许多神经退行性疾病的显著特征。在阿尔茨海默病（AD）中，轴突硬化和变性是普遍存在的，并可能导致AD老年性痴呆的症状。目前在确定轴突损伤对AD的贡献方面的局限性包括由于现有方法的侵入性，无法检测这种损伤何时相对于AD的其他标识符发生。为了克服这一点，我们进一步开发了MRI方法锰增强MRI（MEMRI），以评估体内轴突运输率。在淀粉样蛋白-β（A β）沉积之前，Tg 2576 AD小鼠模型中的轴突运输速率是正常的。随着A β水平的增加和斑块形成之前，我们观察到与对照组相比，Tg 2576小鼠的轴突运输速率显著降低。在空斑形成后，Tg 2576小鼠中转运速率的下降变得更加明显。这些数据表明，在AD的Tg 2576小鼠模型中，在斑块形成之前，体内轴突运输速率降低。(c)2007年爱思唯尔公司All rights reserved.
Axonopathy is a pronounced attribute of many neurodegenerative diseases. In Alzheimer's disease (AD), axonal swellings and degeneration are prevalent and may contribute to the symptoms of AD senile dementia. Current limitations in identifying the contribution of axonal damage to AD include the inability to detect when this damage occurs in relation to other identifiers of AD because of the invasiveness of existing methods. To overcome this, we further developed the MRI methodology Manganese Enhanced MRI (MEMRI) to assess in vivo axonal transport rates. Prior to amyloid-beta (A beta) deposition, the axonal transport rates in the Tg2576 mouse model of AD were normal. As A beta levels increased and before plaque formation, we observed a significant decrease in axonal transport rates of the Tg2576 mice compared to controls. After plaque formation, the decline in the transport rate in the Tg2576 mice became even more pronounced. These data indicate that in vivo axonal transport rates decrease prior to plaque formation in the Tg2576 mouse model of AD. (c) 2007 Elsevier Inc. All rights reserved.